Citation and License

BMC Microbiology 2011, 11:182
doi:10.1186/1471-2180-11-182

Published: 12 August 2011

Abstract

Background

Moraxella catarrhalis, a major nasopharyngeal pathogen of the human respiratory tract, is exposed to rapid
downshifts of environmental temperature when humans breathe cold air. It was previously
shown that the prevalence of pharyngeal colonization and respiratory tract infections
caused by M. catarrhalis are greatest in winter. The aim of this study was to investigate how M. catarrhalis uses the physiologic exposure to cold air to upregulate pivotal survival systems in
the pharynx that may contribute to M. catarrhalis virulence.

Results

A 26°C cold shock induces the expression of genes involved in transferrin and lactoferrin
acquisition, and enhances binding of these proteins on the surface of M. catarrhalis. Exposure of M. catarrhalis to 26°C upregulates the expression of UspA2, a major outer membrane protein involved
in serum resistance, leading to improved binding of vitronectin which neutralizes
the lethal effect of human complement. In contrast, cold shock decreases the expression
of Hemagglutinin, a major adhesin, which mediates B cell response, and reduces immunoglobulin
D-binding on the surface of M. catarrhalis.

Conclusion

Cold shock of M. catarrhalis induces the expression of genes involved in iron acquisition, serum resistance and
immune evasion. Thus, cold shock at a physiologically relevant temperature of 26°C
induces in M. catarrhalis a complex of adaptive mechanisms that enables the bacterium to target their host cellular
receptors or soluble effectors and may contribute to enhanced growth, colonization
and virulence.